ArticleBMC medicine2026
Enhancing oncolytic virotherapy with a tri-specific T-cell engager targeting CD3ε, EpCaM, and 4-1BB: preclinical evaluation and implications for cancer immunotherapy.
Article in BMC medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
Abstract
backgroundCytotoxic T-cell-mediated tumor lysis is a key mechanism of oncolytic virotherapy. While oncolytic viruses expressing bispecific T-cell engagers (BiTE) enhance tumor targeting, they lack costimulatory signals, leading to T-cell exhaustion. We developed an oncolytic adenovirus expressing a trispecific T-cell engager (TriTE) to improve antitumor responses in colorectal carcinoma models.
methodsAn oncolytic adenovirus (Ad5-TriTE) was engineered to express a TriTE molecule targeting EpCAM (tumor antigen), CD3ε (T-cell activation), and 4-1BB (co-stimulation). For comparison, a BiTE-expressing virus (Ad5-BiTE) lacking 4-1BB was used. BiTE (αCD3ε-αEpCAM) facilitates T-cell redirection, whereas TriTE (αCD3ε-α4-1BBL-αEpCAM) adds co-stimulation for enhanced T-cell activation. Antitumor efficacy was evaluated in syngeneic and humanized colorectal carcinoma mouse models.
resultsAd5-TriTE demonstrated efficient tumor infection and TriTE secretion, leading to superior tumor control compared to Ad5-BiTE. Enhanced CD8 + T-cell infiltration and activation correlated with improved antitumor effects in both subcutaneous and peritoneal metastasis models. The humanized version, Ad5-hTriTE, exhibited potent activity in a humanized colon cancer model.
conclusionsOncolytic adenovirus armed with TriTE enhances antitumor immunity by integrating costimulatory signaling. Incorporating costimulatory molecules into oncolytic virotherapy may offer more effective cancer immunotherapy strategies.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.